Abstract
The prevalence of obesity is high among reproductive-age women and is associated with impaired reproductive function. Obesity is multifactorial in origin, yet many cases of obesity result from overconsumption of a diet high in fat. Excess dietary fat increases both adipose and nonadipose tissue lipid content and, through lipotoxicity, leads to cell dysfunction and death. High dietary fat intake, with or without the development of obesity, impairs female hypothalamic-pituitary-ovarian (HPO) axis functionality and fertility. Based on the current evidence, it appears the reproductive dysfunction involves increased leptin and insulin signaling at the various levels of the HPO axis, as well as changes in peroxisome proliferator-activated receptor γ actions and increased inflammation, yet other mechanisms may also be involved. This review summarizes the current body of knowledge on impaired female reproductive function after high-fat diet exposure, as well as discusses proposed mechanisms through which this may occur.